Pype Lobke L, Bertrand Philippe B, Paelinck Bernard P, Heidbuchel Hein, Van Craenenbroeck Emeline M, Van De Heyning Caroline M
Department of Cardiology, Antwerp University Hospital, Antwerp, Belgium.
Genetics, Pharmacology and Physiopathology of Heart, Vasculature and Skeleton (GENCOR) Research Group, University of Antwerp, Antwerp, Belgium.
Front Cardiovasc Med. 2022 Apr 12;9:862044. doi: 10.3389/fcvm.2022.862044. eCollection 2022.
Mitral valve prolapse (MVP) is a common valvular disorder that can be associated with mitral regurgitation (MR), heart failure, ventricular arrhythmias and sudden cardiac death. Given the prognostic impact of these conditions, it is important to evaluate not only mitral valve morphology and regurgitation, but also the presence of left ventricular (LV) function and remodeling. To date, several possible hypotheses have been proposed regarding the underlying mechanisms of LV remodeling in the context of non-syndromic MVP, but the exact pathophysiological explanation remains elusive. Overall, volume overload related to severe MR is considered the main cause of LV dilatation in MVP. However, significant LV remodeling has been observed in patients with MVP and no/mild MR, particularly in patients with bileaflet MVP or Barlow's disease, generating several new hypotheses. Recently, the concept of "prolapse volume" was introduced, adding a significant volume load to the LV on top of the transvalvular MR volume. Another possible hypothesis is the existence of a concomitant cardiomyopathy, supported by the link between MVP and myocardial fibrosis. The origin of this cardiomyopathy could be either genetic, a second hit (e.g., on top of genetic predisposition) and/or frequent ventricular ectopic beats. This review provides an overview of the different mechanisms and remaining questions regarding LV remodeling in non-syndromic MVP. Since technical specifications of imaging modalities impact the evaluation of MR severity and LV remodeling, and therefore might influence clinical decision making in these patients, this review will also discuss assessment of MVP using different imaging modalities.
二尖瓣脱垂（MVP）是一种常见的瓣膜疾病，可伴有二尖瓣反流（MR）、心力衰竭、室性心律失常和心源性猝死。鉴于这些情况对预后的影响，不仅评估二尖瓣形态和反流，而且评估左心室（LV）功能和重塑的存在情况非常重要。迄今为止，关于非综合征性MVP背景下LV重塑的潜在机制已经提出了几种可能的假说，但确切的病理生理学解释仍然难以捉摸。总体而言，与严重MR相关的容量超负荷被认为是MVP中LV扩张的主要原因。然而，在无MR/轻度MR的MVP患者中，尤其是在双叶MVP或巴洛病患者中，已观察到显著的LV重塑，这产生了几种新的假说。最近，引入了“脱垂容积”的概念，在经瓣膜MR容积之上给LV增加了显著的容量负荷。另一种可能的假说是存在伴发性心肌病，MVP与心肌纤维化之间的联系支持了这一点。这种心肌病的起源可能是遗传的、二次打击（例如，在遗传易感性之上）和/或频繁的室性早搏。本综述概述了非综合征性MVP中LV重塑的不同机制和尚存的问题。由于成像方式的技术规格会影响MR严重程度和LV重塑的评估，因此可能会影响这些患者的临床决策，本综述还将讨论使用不同成像方式对MVP的评估。
